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Discontinued Product(±)-HA-966 (Cat. No. 0198) has been withdrawn from sale for commercial reasons.
Biological Activity for (±)-HA-966
The overall effect of this much-investigated compound is the result of the actions of the two enantiomers: glycine-NMDA antagonism by the (+)-isomer and sedative and ataxic effects of the (-)-isomer. See separate isomers 0281 and 0282.
Technical Data for (±)-HA-966
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Product Datasheets for (±)-HA-966
References for (±)-HA-966
References are publications that support the biological activity of the product.
Evans et al (1978) Mg2+-like selective antagonism of excitatory amino acid - induced responses by α,ε-diaminopimelic acid, D-α-aminoadipate and HA-966 in isolated spinal cord of frog and immature rat. Brain Res. 148 536 PMID: 207392
Foster and Kem (1989) HA-966 antagonises NMDA receptors through a selective interaction with the glycine modulatory site. J.Neurosci. 9 2191 PMID: 2542488
Lodge (1989) Non-competitive NMDA antagonists. The NMDA Receptor (2nd edition). Eds. G.L.Collingr 37
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Keywords: (±)-HA-966, (±)-HA-966 supplier, NMDA, Receptors, 0198, Tocris Bioscience
Citations for (±)-HA-966
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Currently there are no citations for (±)-HA-966.
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Huntington's Disease Research Product Guide
This product guide provides a background to Huntington's disease research and lists around 100 products for the study of:
- Somatic Instability
- Proteolysis and Inclusion Bodies
- Transcriptional Dysregulation
- Mitochondrial Dysfunction
- Nuclear-Cytoplasmic Transport Interference
- Stem Cells
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Huntington's Disease Poster
Huntington's disease (HD) is a severe monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the effects of mutant huntingtin aggregation implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
Learning & Memory Poster
Recognition memory enables us to make judgements about whether or not we have encountered a particular stimulus before. This poster outlines the cellular mechanisms underlying recognition memory and its links to long-term depression, as well as the use of pharmacological intervention to assess the role of neurotransmitters in recognition memory.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.
Schizophrenia is a debilitating psychiatric disorder that affects 1% of the worldwide population. This poster describes the neurobiology of Schizophrenia, as well as highlighting the genetic and environmental factors that play a fundamental role in the etiology of the disease. The current and emerging drug targets are also discussed.